Project description:To identify genes that are differentially expressed in the developing mouse embryo as a result of SOX7 deficiency, we performed bulk RNA-seq on Sox7-null and wild-type embryos harvested at E8.5.
Project description:RNA-seq differential gene expression analysis was accomplished in E9.5 pooled(n = approximately 30) microdissected heart tubes from Sox7-null embryos and a wild-type littermates.
Project description:Transcriptomic analyses of yolk sacs from mouse embryos at E8.5 was performed to assess the dosage dependent effects of varying Etv2 dosage on early endothelial and hematopoietic development.
Project description:The object of this study was to identify genes transcriptionally upregulated and downregulated in response to Tcof1 haploin-sufficiency during mouse embryogensis Experiment Overall Design: Total RNA was extracted from 3 E8.5 wild-type and 3 E8.5 Tcof1+/- littermate embryos using the RNeasy Mini Protocol for Isolation of Total RNA from Animal Tissues (Qiagen) according to the manufacturerâs protocol. RNA quality and quantity was determined using the Bioanalyser. To generate targets for microarray analysis, total RNA (100 ng) from each wild-type and mutant embryo was amplified using Two-Cycle Target Labeling (Affymetrix) according to the manufacturerâs instructions. Biotinylated target cRNAs (20 μg) from the 3 wild-type and 3 Tcof1+/- embryos were hybridised to separate GeneChip® Mouse Genome 430 2.0 arrays (Affymetrix), following standard Affymetrix procedures.
Project description:The effects of loss of the large neutral amino acid transporter Slc7a5 (aka Lat1) on mouse embryonic development were investigated. Slc7a5 fl/fl mice harbouring two copies of the Slc7a5 targeted allele (exon 1 of Slc7a5 flanked with two loxP sites), were crossed with a mouse line ubiquitously expressing cre recombinase under the Bal1 promoter (Bal1-cre) to obtain a global Slc7a5 knockout mouse (Poncet et al. 2014 PLoS One 9: e89547). Heterozygous Slc7a5+/- C57Bl/6 mice were viable and fertile and were bred free of Bal1-cre in subsequent generations. Slc7a5 -/- embryos were obtained by inter-crossing heterozygotes and a phenotype was apparent by E9.5. To identify the first cellular processes affected by Slc7a5 loss RNAseq was carried out to compare transcriptomes of null and wildtype E8.5 embryos.